Study: Boosting Neural Pathway from Gut to Brain Could Play Part in Weight Control
Targeted News Service
"By increasing the nerve fibers that send messages to the brain, we found less food was consumed during a meal," said
The study is published in
The researchers studied a mouse model with a targeted knockout of the brain-derived neurotrophic factor gene that decreases levels of this nerve growth factor in the gastrointestinal tract. Suprisingly, they found these mice had an increase in vagal sensory innervation of the gastrointestinal tract and ate small meals.
"The small meals likely resulted because the increased innvervation led to an increase in neural signals telling the brain the stomach is full," Fox said.
Brain-derived neurotrophic factor is involved in controlling the development of sensory pathways of the vagus nerve. This nerve feeds the brain sensory information related to the types of nutrients present in the gastrointestinal tract as well as to muscle contractions and distensions associated with digestion.
Fox said the possible implication for humans someday is stimulation of the vagus nerve to reduce the amount people eat, but more research and clinical work is needed. Electrical stimulation of the vagus nerve used to treat epilepsy and depression in patients that don't respond to medications has been found to reduce body weight in some of them, and the current study suggests this effect might result in part from eating smaller meals as opposed to only eating fewer meals or increasing metabolism.
"Treating people so they eat smaller meals is just one component of addressing obesity and may not be enough in itself," said Fox, who is affiliated with
Reduced Intestinal Brain-Derived Neurotrophic Factor Increases Vagal Sensory Innervation of the Intestine and Enhances Satiation
Brain-derived neurotrophic factor (BDNF) is produced by developing and maturing gastrointestingal (GI) tissues that are heavily innervated by autonomic neurons and may therefore control their development or function. To begin investigating this hypothesis, we compared the morphology, distribution, density of intraganglionic laminar endings (IGLEs), the predominant vagal GI afferent, in mice with reduced INT-BDNF-/- and controls. Contrary to expectations of reduced development, IGLE density and longtidunal axon bundle number in the intestine of INT-BDNF-/-mice were increased, but stomach IGLEs were normal. INT-BDNF-/-mice also exhibited increased vagal sensory neuron numbers, suggesting that their survival was endhanced. To determine whether increased intestinal IGLE density or other changes to gut innervation in INT-BDNF-/-mice altered feeding behavior, meal pattern and microstructural analyses were performed. INT-BDNF-/-mice ate meals of much shorter duration than controls, resulting in reduced meal size. Increased suppression of feeding in INT-BDNF-/-mice during the late phase of a scheduled meal suggested that increased satiation signaling contributed to reduced meal duration and size. Furthermore, INT-BDNF-/-mice demonstrated increases in total daily intermeal interval and satiety ratio, suggesting that satiety signaling was augmented. Compensatory responses maintained normal daily food intake and body weight in INT-BDNF-/-mice. These findings suggest a target organ-derived neurotrophin suppresses development of that organ's sensory innervation and sensory neuron survival and demonstrate a role for BDFN produced by peripheral tissues in short-term controls of feeding, likely through its regulation of development or function of gut innervation, possibly including augmented intestinal IGLE innervation.
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